A study of the effect of carbon nanodots on TNF-a induced human aortic endothelial inflammation

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Urooj Amin (Creator)
Institution
The University of North Carolina at Greensboro (UNCG )
Web Site: http://library.uncg.edu/
Advisor
Zhenquan Jia

Abstract: Atherosclerosis, a prevalent contributor to cardiovascular disease (CVD) on a global scale, is primarily triggered by inflammation, which plays a critical role in initiating the disease process. This inflammatory response leads to endothelial cell dysfunction or damage, ultimately resulting in the formation of plaque buildup within the inner walls of arteries. The emerging nanomaterials provide new prospects to lower the economic and healthcare costs associated with CVD. Carbon nanodots (CNDs), a type of nanoparticle, are particularly attractive due to their biocompatibility, fluorescent capabilities, and potential antioxidant properties. While much research has been conducted on the use of CNDs as bioimaging and drug-delivery tools, their potential anti-inflammatory effects, particularly in the cardiovascular system, have yet to receive much attention. The aorta is particularly vulnerable to atherosclerosis, being the largest affected area. In this study, HAEC (human aortic endothelial cells) were chosen as the cell line due to their capability to express endothelial cell surface biomarkers, and their common use in vascular research has provided a comprehensive understanding of cell lines. However, the impact of CNDs on HAEC has not been investigated yet. In this study, the impact of CNDs on TNF-a induced inflammation in HAEC was studied. Our results demonstrate CNDs inhibited the production of inflammatory genes, such as IL-8, E-Selectin, and CCL2, in vitro in response to TNF-a. With concentrations of up to 0.6 mg/mL used, CNDs did not show any cytotoxic capabilities in our results in HAEC. Fluorescence microscopy data indicated that HAEC were able to uptake CNDs at the concentrations used. The NF-?B Luciferase Reporter Cell assay results showed that CNDs have the ability to reduce TNF-a-mediated increase in NF-kB activity. The results of the Nrf2 pathways also indicated that CNDs can activate Nrf2 transcription, thus leading to an increase in Nrf2-mediated upregulation of various antioxidant genes, including HO-1, GCLC, NQO-1, and GR. Through these results, it can be suggested that the anti-inflammatory effects of CNDs can be related to the downregulation of the NF-?B pathway and the up-regulation of the Nrf2 pathway signaling. This is the first study to examine the effects of CNDs on human aorta endothelial inflammation. [This abstract may have been edited to remove characters that will not display in this system. Please see the PDF for the full abstract.]

Additional Information

Publication
Thesis
Language: English
Date: 2023
Keywords
Carbon Nanodots, Endothelial Inflammation, Molecular Toxicology
Subjects
Atherosclerosis
Endothelial cells
Inflammation
Nanoparticles

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